Notice of Pre-AIA or AIA Status The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA. DETAILED ACTION Status of Application/Election/Restrictions Applicant’s election without traverse of Group I (claims 1-8), Alzheimer’s disease, agonistic anti-Dectin-1 antibody and decreased microglial autophagy in the reply filed on June 17, 2025 is acknowledged. Claims 1-20 are pending in this application . Upon reconsideration, the restriction requirement among Groups I-III and the species election among different effects recited in claims 4-6, 11 and 13 in the office action dated April 17, 2025 are withdrawn. The subject matter to the extent of claims 4-6 and 9-20 is included and under examination in this office action. Election was made without traverse in the reply filed on June 17, 2025 . Claims 1-20 are under examination with respect to Alzheimer’s disease (AD) , agonistic anti-Dectin-1 antibody and decreased microglial autophagy in this office action. Priority Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) is acknowledged. Applicant has not complied with one or more conditions for receiving the benefit of an earlier filing date under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, or 365(c) as follows: The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of the first paragraph of 35 U.S.C. 112. See Transco Products, Inc. v. Performance Contracting, Inc. , 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994). The disclosure of the prior-filed application s , provisional Application 62/529753, Application No. 16/030793 and Application No.17395357 , fail to provide adequate support or enablement in the manner provided by the first paragraph of 35 U.S.C. 112 for one or more claims of this application. The instant application claims methods for treating a microglial dysfunction-associated neurodegenerative disease including Alzheimer’s disease or characterized by mutation in Trem2 affecting microglial functions using a microglia receptor agonist that directly activates SYK or activates at least one ITAM pathway , which are not presented in the provisional Application 62/529753 filed Jul 7, 2017, Application No. 16/030793 filed Jul 09, 2018, or Application No.17395357 filed Aug 05, 2021 . The methods of using a microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway w ere only disclosed in the instant Application No. 17/840368 filed on Jun 14, 2022 (see p.12 of the specification.). Therefore, the priority for the subject matter related to methods of treating microglial dysfunction-associated neurodegenerative disease including Alzheimer’s disease or characterized by mutation in Trem2 affecting microglial functions using a microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway in the instant application is Jun 14, 2022 . Specification The disclosure is objected to because of the following informalities: The use of the term “Eponate”, “Leica Ultracut UCT” “JEOL” “AMT” (p. 86) “MATLAB: “TO-PRO-3” (p. 87; p.92) “Illumina NovaSeq” (p.90), “EXpi293F”, “miRNeasy” “SYBR Green”, “LightCycler” (p. 91) , which is a trade name or a mark used in commerce, has been noted in this application. The term should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term . Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks. Appropriate correction is required. Claim Objections Claims 1, 3-4 , 7, 9 -10, 14, 16, 18-19 are objected to because of the following informalities: The recitations “SYK”, “TREM2” , “CLEC7A” and “ITAM” are not unique or common abbreviation s in the art. Applicants are required to spell out “SYK”, “TREM2” , “CLEC7A” and “ITAM” at the first usage. In addition, the gene symbol of “ Trem2 ” recited in claims 4, 9 and 16 should be italic. Appropriate correction is required. Claim Rejections - 35 USC § 112 7. The following is a quotation of 35 U.S.C. 112(b): (b ) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention. The following is a quotation of 35 U.S.C. 112 (pre-AIA), second paragraph: The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the appl icant regards as his invention. Claim s 4-6 and 9-20 are FILLIN "Enter claim indentification information" \* MERGEFORMAT rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor, or for pre-AIA the applicant regards as the invention. Claims 4-6, 9-20 are indefinite because: i. The term " decreased ” , “improved” or “reduced” in claims 4-6 and 11 is a relative term which renders the claim indefinite. The term " decreased ” , “improved” or “reduced” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. Applicant fails to set forth the metes and bounds of what is encompassed within the definition of " decreased ” , “improved” or “reduced” ”. Since the metes and bounds are unknown, a skilled artisan cannot envision what would be considered as " decreased microglial activity ” , “improved microglial metabolic activity”, “decreased microglial autophagy”, “recued neurite dystrophy”, “decreased cell death”, “improved microglia viability” or “improved microglia numbers” recited in the claim. Thus the claim s are indefinite. ii. The recitation “a mutation in Trem2 affecting microglial functions” recited in claims 9 and 16 is not defined . A mutation in Trem2 can increase, enhance or reduce, abolish or inhibit a specific microglial function or activity . Since Applicant has not limited the mutation, the activity or function of microglia and how the mutation affect the microglia function and how the microglia-dysfunction is associated with what specific neurodegenerative disease, a skilled artisan cannot envision what mutation in Trem2 is affecting what microglial functions and what and neurodegenerative disease is associated with the recited mutation in Trem2 affecting microglial functions and within the scope of the claims , which renders the claims indefinite. iii. The rest of claims are indefinite as depending from an indefinite claim. Claim Rejections - 35 USC § 112 8 . The following is a quotation of the first paragraph of 35 U.S.C. 112(a): (a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention. The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112: The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention. Claim s 1-20 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, because the specification, while being enabling for decreasing the number of LC3 + and cleaved caspase-3 + microglia, increasing microglia/high powered field (HPF) in plaque-bearing regions of the cortex and clustering of microglia around plaques and mitigating autophagy and death of microglia in Trem2 -/- 5XFAD mice treated with cyclocreatine compared to untreated the Trem2 -/- 5XFAD mice by administering cyclocreatine to the Trem2 -/- 5XFAD mic e or increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice (i.e. 5xFAD mice with hypofunctional TREM2 R47H , which are mice that express the defective TREM2 R47H allele and accumulate Aβ plaques ) treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice by administering to the TREM2 R47H 5xFAD mice an agonistic anti- CLEC7A monoclonal antibody 2A11, does not reasonably provide enablement for method s for treating all forms of microglial dysfunction-associated neurodegenerative disease including AD or characterized by a undefined mutation in Trem2 affecting microglial functions using the claimed structurally and functionally undefined microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway as broadly claimed. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. “There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is ‘undue’. These factors include, but are not limited to: (A) The breadth of the claims; (B) The nature of the invention; (C) The state of the prior art; (D) The level of one of ordinary skill; (E) The level of predictability in the art; (F) The amount of direction provided by the inventor; (G) The existence of working examples; and (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. In re Wands , 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)”. See MPEP § 2164.01. Claims 1- 8 are drawn to a method for treating a microglial dysfunction-associated neurodegenerative disease in a subject in need thereof , comprising administering to the subject a therapeutically effective amount of a composition comprising a microglial receptor agonist that directly activates SYK . Claims 9 - 15 are drawn to a method of reversing neuronal damage in a subject having a microglial dysfunction-associated neurodegenerative disease characterized by a mutation in Trem2 affecting microglial functions, comprising administering to the subject a therapeutically effective amount of a composition comprising a microglial receptor agonist that directly activates SYK. Claims 1 6 -2 0 are drawn to a method of treating at least one symptom of cognitive dysfunction in a subject having a microglial dysfunction-associated neurodegenerative disease characterized by a mutation in Trem2 affecting microglial functions, comprising administering to the subject a therapeutically effective amount of a composition comprising a microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway. The claims encompass treating all forms of undefined microglial dysfunction-associated neurodegenerative dis eases and CNS degenerative diseases including AD using a structurally and functionally undefined microglia receptor agonist that directly activates SYK including a structurally and functionally undefined CLEC7A agonist or pharmaceutically acceptable salt thereof. In addition, claims 9-15 encompass regenerating or reversing different forms of lesioned/damaged neurons caused by all possible mechanisms by the claimed microglia receptor agonist or CLEC7A agonist. The instant invention is based on findings that : i) administration of cyclocreatine to Trem2 −/− 5XFAD mice mitigated autophagy and death of microglia in Trem2 −/− 5XFAD mice treated with cyclocreatine as compared to untreated Trem2 −/− 5XFAD mice (see Example 6 , Figures 6-7 ). ii) SYK-deficient microglia in Syk . ∆ MG -5xFAD mice are unable to enclose Aβ aggregates, resulting in increase of Aβ plaque pathology and accelerated behavioral deficits (Figures 13-18) . Both Trem2 −/− -5xFAD and Syk ∆ MG -5xFAD mice had a reduced percentage of ApoE + plaques compared to controls but the reduction in ApoE + plaques in Trem2 −/− -5xFAD mice is more than in Syk ΔMG -5xFAD mice (see Figures 18 ) iii) intraperitoneal administration of a n agonistic anti- CLEC7A monoclonal antibody 2A11 to TREM2 R47H 5xFAD mice (i.e. 5xFAD mice with hypofunctional TREM2 R47H , which are mice that express the defective TREM2 R47H allele and accumulate Aβ plaques ) increased density of plaque-associated microglia and Iba1 and CD11c staining (see Figure 19; Note that CLEC7A is also called dectin-1, a receptor that directly activates SYK ) . Applicant extrapolates the above findings to the claimed methods for treating a microglial dysfunction-associated neurodegenerative disease in a subject in need thereof, reversing neuronal damage in a subject having a microglial dysfunction-associated neurodegenerative disease characterized by a mutation in Trem2 affecting microglial functions and treating at least one symptom of cognitive dysfunction in a subject having a microglial dysfunction-associated neurodegenerative disease characterized by a mutation in Trem2 affecting microglial functions by administering to the subject a composition comprising a microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway. B ased on the specification and the prior art, Applicant is enabled for a method of decreasing the number of LC3 + and cleaved caspase-3 + microglia, increasing microglia/high powered field (HPF) in plaque-bearing regions of the cortex and clustering of microglia around plaques and mitigating autophagy and death of microglia in Trem2 -/- 5XFAD mice treated with cyclocreatine compared to untreated the Trem2 -/- 5XFAD mice by administering cyclocreatine to the Trem2 -/- 5XFAD mice, or a method of increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice (i.e. 5xFAD mice with hypofunctional TREM2 R47H , which are mice that express the defective TREM2 R47H allele and accumulate Aβ plaques ) treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice by administering to the TREM2 R47H 5xFAD mice an structurally and functionally defined agonistic anti- CLEC7A monoclonal antibody 2A11. However, t he instant claims are not limited to the agents and methods set forth above but also encompass treatment of all forms of microglial dysfunction-associated neurodegenerative diseases or microglial dysfunction-associated neurodegenerative diseases characterized by all possible mutations in Trem2 affecting all possible microglial functions including AD caused by all possible mechanisms and using a structurally and functionally undefined microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway including a structurally and functionally undefined CLEC7A agonist. T he specification provide s in sufficient guidance to enable one of skill in the art to practice the full scope of the claimed invention without undue experimentation because of the complexity and the unpredictability of the diseases , and failure of provid ing evidence to support a correlation between the Trem2 -/- 5XFAD mice or TREM2 R47H 5xFAD mice and the pathogeneses or causes of all forms of microglial dysfunction-associated neurodegenerative diseases or microglial dysfunction-associated neurodegenerative diseases characterized by all possible mutations in Trem2 affecting all possible microglial functions including AD caused by all possible mechanisms in vivo in view of Henstridge et al. ( Nat. Rev. Neurosci. 2019; 20: 94-107 ) , Tayebati (see p. 106, 1 st col, 2nd paragraph, Tayebati, Mech. Ageing Dev. 2006. 127: 100-8) and Sarter (see p. 645, abstract, Sarter, Neurosci. and Biobehav. Rev. 2004. 28: 645-650). The specification provide s no guidance as to what the structural and functional relationship between the claimed microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway or the claimed CLEC7A agonist and the agonistic anti- CLEC7A monoclonal antibody 2A11 increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice treated with the agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice shown in Examples of the specification , indicating undue experimentation is required by a skilled artisan to perform while practicing the claimed invention. The specification also provide s no guidance as to what the structural and functional relationship between the claimed microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway or the claimed CLEC7A agonist and the cyclocreatine in decreasing the number of LC3 + and cleaved caspase-3 + microglia, increasing microglia/high powered field (HPF) in plaque-bearing regions of the cortex and clustering of microglia around plaques and mitigating autophagy and death of microglia in Trem2 -/- 5XFAD mice treated with cyclocreatine compared to untreated the Trem2 -/- 5XFAD mice , indicating undue experimentation is required by a skilled artisan to perform while practicing the claimed invention. The causes of different forms of microglial dysfunction-associated neurodegenerative diseases or microglial dysfunction-associated neurodegenerative diseases characterized by a mutation in Trem2 affecting microglial functions including AD caused by all possible mechanisms are different. For example, there are many factors involved in molecular mechanisms contributing to the formation of -amyloid deposits and neurofibrillary tangles in AD. They include genetic mutations affecting the processing of APP or other molecules involved in protein processing and targeting in view of Henstridge et al. (see p. 94), Tayebati (see p. 106, 1 st col, 2nd paragraph) and Sarter (see p. 645, abstract). Each type of animal models of microglial dysfunction-associated neurodegenerative diseases or microglial dysfunction-associated neurodegenerative diseases characterized by a mutation in Trem2 affecting microglial functions caused by all possible mechanisms or each type of animal models of AD only reflects part of pathogenesis of the disease as taught by Tayebati (see p. 106, 1 st col, 2nd paragraph) and Sarter (see p. 645, abstract). Applicant obviously intended to treat all forms of microglial dysfunction-associated neurodegenerative diseases or microglial dysfunction-associated neurodegenerative diseases characterized by a mutation in Trem2 affecting microglial functions including all forms of AD caused by all possible mechanisms using the claimed microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway or the claimed CLEC7A agonist . However, the specification fails to provide a well-established correlation among different forms of microglial dysfunction- associated neurodegenerative diseases including different forms of AD or characterized by a mutation of Trem2 affecting microglial functions caused by all possible mechanisms. The specification fails to establish that different forms of microglial dysfunction-associated neurodegenerative diseases including different forms of AD or characterized by a mutation of Trem2 affecting microglial functions caused by all possible mechanisms can be treated by the same drugs or same conditions or have the same effects in response to the same drugs. Thus, it is unpredictable whether one treatment for one specific disorder can be applied to another disorder, indicating undue experimentation is required by a skilled artisan to perform while practic ing the claimed invention. While the skill level in the art is high, the level of predictability is low. The molecular mechanisms underlying cognitive dysfunction or dementia of AD are unclear (see p. 94; Henstridge et al. Nat. Rev. Neurosci. 2019; 20: 94-107). The specification provides insufficient guidance to demonstrate that administration of the claimed microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway or the claimed CLEC7A agonist can treat cognitive dysfunction or dementia in AD because Abeta accumulation and/or hyperphosphorylated tau is not the only cause of cognitive dysfunction or dementia in AD. Several factors and genes are involved in pathogenesis of AD including ageing, inflammation and immune response, APP, presenilin1/2, ApoE and genes involved in the amyloid cascade, genes involved in the mitochondrial cascade as taught by Swerdlow (p. 348-344, Swerdlow, Clin. Interv. Ageing 2007; 2:347-359), Atwood et al. (p. 33, abstract; Atwood et al., J. Alzheimer’s Disease; 2015; 47:33-47) and Henstridge et al. (p. 95-103; Henstridge et al., Nat. Rev. Neurosci. 2019; 20: 94-107). In addition, it is known that fully developed animal models for neurodegenerative diseases are still lacking especially for AD because the complexity of the disease and deficiency of characterized cognition (see p. 403, abstract. Anger. Neurotoxicology 1991. 12: 403-13). For example, the animal model of brain amyloidosis induced by acute or infusion of A b as described in the instant case could only be used to screening for inhibiting the formation of A b but not for evaluating the generation of A b by the effects of b -and g -secretase, which is another molecular mechanism for the pathogenesis of AD (see p. 106, 1 st col, 2nd paragraph, Tayebati. Mech. Ageing Dev. 2006. 127: 100-8). The art also recognizes that although the Morris water maze behavioral test is a popular choice used in studies determining effects of learning and memory, the test has been disappointing in the predictive validity of data from animal tests on learning and memory used to discover and characterize drugs for the treatment of cognitive impairment and dementia in clinical testing. The animal tasks generate a high rate of false positive (see p. 646, 2nd col. 2nd paragraph) and the validity of the test itself is also a part of the research process (see p. 645, abstract, Sarter. Neurosci. and Biobehav. Rev. 2004. 28: 645-650). Thus, in order to closely reflect the data obtained from animal models to the real situation of Alzheimer’s disease in humans, it has been proposed that a rodent model should include 1) tests currently used to identify in rodents deficits associated with AD; 2) tests to identify Alzheimer-related signs in patients; and 3) tests that relate to theoretical constructs of human and animal cognition, which should include at least spatial learning and memory (such as Morris Water Maze and Radial Arm Maze), delayed recall match-to-sample, serial response learning, and visual discrimination (such as vertical vs. horizontal stimuli).(see p. 403, abstract. Anger. Neurotoxicology 1991. 12: 403-13). Applicant is enabled for increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice (i.e. 5xFAD mice with hypofunctional TREM2 R47H , which are mice that express the defective TREM2 R47H allele and accumulate Aβ plaques ) treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice by administering to the TREM2 R47H 5xFAD mice an structurally and functionally defined agonistic anti- CLEC7A monoclonal antibody 2A11. Applicant is also enabled for decreasing the number of LC3 + and cleaved caspase-3 + microglia, increasing microglia/high powered field (HPF) in plaque-bearing regions of the cortex and clustering of microglia around plaques and mitigating autophagy and death of microglia in Trem2 -/- 5XFAD mice treated with cyclocreatine compared to untreated the Trem2 -/- 5XFAD mice by administering cyclocreatine to the Trem2 -/- 5XFAD mice. However, the specification fails to provide sufficient guidance or evidence to demonstrate that all forms of microglial dysfunction-associated neurodegenerative diseases or characterized by a mutation of Trem2 affecting microglial functions caused by all possible mechanisms including AD caused by different mechanisms can be treated by the claimed microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway or the claimed CLEC7A agonist because there is no well-established correlation between increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 as compared to untreated TREM2 R47H 5xFAD mice and the pathogeneses or causes of AD caused by other mechanisms or microglial dysfunction-associated neurodegenerative diseases caused by other mechanisms. Since the pathogenesis of AD or other microglial dysfunction-associated neurodegenerative diseases is complex and the causes of dementia/cognitive dysfunction in AD have not been deciphered and are equally complex, it is unpredictable whether increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice can be applied to other forms of AD caused by other mechanisms or other microglial dysfunction-associated neurodegenerative diseases caused by other mechanisms , indicating that undue experimentation is required by a skilled artisan to perform while practicing the claimed invention. Further, Applicant fails to provide sufficient guidance to enable a skilled artisan to practice the invention of claims 9-15 without undue experimentation because the claims encompass nerve or neurite regeneration of the CNS in vivo and regeneration from a mature lesioned neuron of the CNS in vivo . It is known in the art that t he regeneration in the central nervous system is still a challenge. Several molecules have been identified to inhibit remyelination in the CNS and axonal/neurite regeneration, myelin-associated molecules such as Nogo, MAG, and proteoglycans in the extracellular matrix, (see p. 1052, 2 nd col., Blight Nat. Neurosci. 2002. 5: 1051-4; p. 316, Schmidt et al. Annu. Rev. Biomed. Eng. 2003. 5: 293-347 and p. 450, 2 nd col. Hoke et al. Nat. Clin. Pract. Neurol. 2006: 448-454). The nerve injury of the CNS in vivo results in generation of glial scars, which inhibits nerve regeneration of the CNS (Hoke et al. Nat. Clin. Pract. Neurol. 2006: 448-454). Neither the specification nor the prior art teaches that degeneration of the CNS in vivo can be regenerated by any given agent . T he specification fails to provide sufficient guidance or evidence to demonstrate that administration of the claimed microglia receptor agonist or CLEC7A agonist can reverse neuronal damage in a subject with microglial dysfunction-associated neurodegenerative disease s or AD because mature neurons in the CNS or in patients with CNS neurodegenerative diseases or microglial dysfunction-associated neurodegenerative diseases once are damaged, they cannot reverse or regenerated Moreover , the specification fails to provide sufficient guidance as to what other microglial receptor agonists that directly activate SYK or activate at least one ITAM pathway or other CLEC7A agonists are and whether other microglial receptor agonists that directly activate SYK or at least one ITAM pathway or other CLEC7A agonists can be used in the claimed method because the specification provides no structural and functional relationship or correlation between the claimed microglial receptor agonists/CLEC7A agonists and the agonistic anti- CLEC7A monoclonal antibody 2A11 used in TREM2 R47H 5xFAD mice or cyclocreatine used in the Trem2 -/- 5XFAD mice and shown Examples of the instant specification. The specification fails to teach what specific or common structures/amino acid sequences are and can be included in all microglial receptor agonists that directly activate SYK or activate at least one ITAM pathway or all CLEC7A agonists in order to preserve the activity of agonistic anti- CLEC7A monoclonal antibody 2A11 in increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice treated with the agonistic anti- CLEC7A monoclonal antibody 2A11 as compared to untreated TREM2 R47H 5xFAD mice or even treating all forms of AD or all forms of microglial dysfunction-associated neurodegenerative diseases including characterized by a mutation in Trem2 affecting microglia function or AD caused by all possible mechanisms , indicating undue experimentation is required by a skilled artisan to preform while practicing the claimed invention. Therefore, in view of the breadth of the claims, the lack of guidance in the specification, the limited examples, the unpredictability of inventions, and the current status of the art, undue experimentation would be required by one of skill in the art to perform in order to practice the full scope of the claimed invention as it pertains to method s for treating a microglial dysfunction-associated neurodegenerative disease including characterized by a mutation in Trem2 affecting microglial functions and treating at least one symptom of cognitive dysfunction thereof and reversing neuronal damage in a subject having a microglial dysfunction-associated neurodegenerative disease including characterized by a mutation in Trem2 affecting microglial functions by the claimed microglia receptor agonist that directly activates SYK, or at least one ITAM pathway or the claimed CLEC7A agonist. Claim Rejections - 35 USC § 112 9 . Claim s 1-20 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention. To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof. Claims 1- 20 encompass using a genus of microglial receptor agonist that directly activates SYK or a genus of microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway for treating a genus of microglial dysfunction-associated neurodegenerative disease or a genus of microglial dysfunction-associated neurodegenerative disease characterized by a genus of mutation in Trem2 affecting a genus of microglial functions. A pplicant has not disclosed sufficient species for the broad genus of microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway, the broad genus of microglial dysfunction-associated neurodegenerative disease or the broad genus of mutation in Trem2 affecting the broad genus undefined microglial functions. The specification only describes i) administration of cyclocreatine to Trem2 −/− 5XFAD mice mitigated autophagy and death of microglia in Trem2 −/− 5XFAD mice treated with cyclocreatine as compared to untreated Trem2 −/− 5XFAD mice (see Example 6, Figures 6-7);ii) intraperitoneal administration of a n agonistic anti- CLEC7A monoclonal antibody 2A11 to TREM2 R47H 5xFAD mice (i.e. 5xFAD mice with hypofunctional TREM2 R47H , which are mice that express the defective TREM2 R47H allele and accumulate Aβ plaques ) increased density of plaque-associated microglia and Iba1 and CD11c staining (see Figure 19; Note that CLEC7A is also called dectin-1, a receptor that directly activates SYK ) . However, the claims are not limited to the agent and method set forth above but also encompass using a genus of structurally and functionally undefined microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway for treating a genus of undefined microglial dysfunction-associated neurodegenerative disease including microglial dysfunction-associated neurodegenerative disease characterized by a genus of undefined mutations in Trem2 affecting a genus of undefined microglial functions in a subject. . In making a determination of whether the application complies with the written description requirement of 35 U.S.C. 112, first paragraph, it is necessary to understand what Applicant is in possession of and what Applicant is claiming. M.P.E.P. § 2163 instructs: An invention described solely in terms of a method of making and/or its function may lack written descriptive support where there is no described or art-recognized correlation between the disclosed function and the structure(s) responsible for the function. . . . An applicant may show possession of an invention by disclosure of drawings or structural chemical formulas that are sufficiently detailed to show that applicant was in possession of the claimed invention as a whole. . . . An applicant may also show that an invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics which provide evidence that applicant was in possession of the claimed invention, i.e., complete or partial structure, other physical and/or chemical properties, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics.” This standard has not been met in this case. From the specification, Applicant is possession of using a structurally and functionally defined agonistic anti- CLEC7A monoclonal antibody 2A11 for increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice . However, Applicant is not in possession of using other structurally and functionally undefined microglial receptor agonists that directly activate SYK or at least one ITAM pathway or other structurally and functionally undefined CLEC7A agonists for increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice or even treating a genus of undefined microglial dysfunction-associated neurodegenerative disease including microglial dysfunction-associated neurodegenerative disease characterized by a genus of undefined mutations in Trem2 affecting a genus of undefined microglial functions . The specification provide s no identification of any particular portion of the structure that must be conserved. The instant specification fails to provide sufficient descriptive information, such as definitive structural or functional features of the claimed genus of microglial receptor agonists that directly activate SYK or at least one ITAM pathway or the genus of CLEC7A agonists. There is no description of the conserved regions which are critical to the function of the claimed genus. There is no information regarding the relation of structure of other microglial receptor agonists that directly activate SYK or at least one ITAM pathway or other CLEC7A agonists to the function of the agonistic anti- CLEC7A monoclonal antibody 2A11 in increasing density of plaque-associated microglia and Iba1 and CD11c staining in TREM2 R47H 5xFAD mice treated with an agonistic anti- CLEC7A monoclonal antibody 2A11 compared to untreated TREM2 R47H 5xFAD mice or even treating a undefined microglial dysfunction-associated neurodegenerative disease including microglial dysfunction-associated neurodegenerative disease characterized by a undefined mutation in Trem2 affecting undefined microglial function s . There is also no information regarding the relation of structure of the undefined mutation in Trem2 affecting undefined microglial function and the function of TREM2 R47H 5xFAD mice . There is no information regarding the correlation of microglial dysfunction-associated neurodegenerative disease characterized by an undefined mutation in Trem2 affecting undefined microglial function and T REM2 R47H 5xFAD mice Furthermore, the prior art does not provide compensatory structural or correlative teachings sufficient to enable one of skill to identify what microglial dysfunction-associated neurodegenerative disease including microglial dysfunction-associated neurodegenerative disease characterized by a undefined mutation in Trem2 affecting undefined microglial functions are, and what other microglial receptor agonists that directly activate SYK or at least one ITAM pathway or other CLEC7A agonists might be and what other mutation in Trem2 affecting microglial functions might be . Since the common characteristics/features of microglial dysfunction-associated neurodegenerative disease including microglial dysfunction-associated neurodegenerative disease characterized by a undefined mutation in Trem2 affecting undefined microglial functions, and other microglial receptor agonists, other CLEC7A agonists and other mutations in Trem2 affecting microglial functions are unknown, a skilled artisan cannot envision the functional correlations of the genus with the claimed invention. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the genus of microglial dysfunction-associated neurodegenerative disease , microglial receptor agonists, CLEC7A agonist, mutations in Trem2 affecting microglial functions and microglial dysfunction-associated neurodegenerative disease characterized by an undefined mutation in Trem2 affecting undefined microglial functions . Based on MPEP § 2161.01 and §2163, “ t o satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116 ” . Vas-Cath Inc. v. Mahurkar , 19USPQ2d 1111, clearly states “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention . The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed. ” (See page 1117.) The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed.” (See Vas-Cath at page 1116). As discussed above, the skilled artisan cannot envision the detailed chemical structure of the encompassed genus of microglial dysfunction-associated neurodegenerative disease , microglial receptor agonists, CLEC7A agonist, mutations in Trem2 affecting microglial functions and microglial dysfunction-associated neurodegenerative disease characterized by an undefined mutation in Trem2 affecting undefined microglial functions , and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. The compound itself is required. See Fiers v. Revel , 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd. , 18 USPQ2d 1016. One cannot describe what one has not conceived. See Fiddes v. Baird , 30 USPQ2d 1481 at 1483. Therefore, the claimed methods ha ve not met the written description provision of 35 U.S.C. §112, first paragraph. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. §112 is severable from its enablement provision (see page 1115). Applicant is directed to the Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, ¶ 1 "Written Description" Requirement. See MPEP § 2161.01 and 2163. 10 . In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status. Claim Rejections - 35 USC § 102 11. The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action: A person shall be entitled to a patent unless – (a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention. (a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention. Claims 1- 20 are rejected under 35 U.S.C. 102(a)(2) as being anti cipated by Fotakis et al. (US12037399, issued on Jul 16, 2024, priority Oct 7, 2020) . Claims 1- 8 are drawn to a method for treating a microglial dysfunction-associated neurodegenerative disease including AD in a subject in need thereof, comprising administering to the subject a therapeutically effective amount of a composition comprising a microglial receptor agonist that directly activates SYK. Claims 9 - 20 are drawn to method s of treating at least one symptom of cognitive dysfunction and reversing neuronal damage in a subject having a microglial dysfunction-associated neurodegenerative disease characterized by a mutation in Trem2 affecting microglial functions including AD, comprising administering to the subject a therapeutically effective amount of a composition comprising a microglial receptor agonist that directly activates SYK or activates at least one ITAM pathway. Fotakis et al. (US12037399) teach a method of treating a disease including amyloidosis, an ageing-related disease or disorder including AD (col.) , comprising administering to a subject in need thereof a composition comprising an agonistic anti-human Dectin-1 antibody having a VH and a VL, wherein the VH comprises SEQ ID NOs: 1-3 for HCDRs1-3 and the VL comprises SEQ ID NOs; 4-6 for LCDRs1-3 or wherein the VH comprises SEQ ID NO:7 and the VL comprises SEQ ID NO:8 (see col. 62, lines 45-50; col. 67-68; col.70, lines 9-19; col. 92-93, Example 15; col. 73-74, Examples 4-5; col. , claims 1-97). The agonistic anti-human Dectin-1 antibody disclosed by Fotakis is a CLEC7A agonist as recited in claims 7, 14 and 19 because CLEC7A is also called Dectin-1 , and the agonistic anti-Dectin-1 antibody is a microglial receptor agonist that directly activates SYK or comprises a CLEC7A agonist as recited in claims 1, 7, 9, 14, 16, and 19 as evidenced by paragraphs [0213] and [0240], [0053]-[0056] of the instant specification (based on the published application) . Fotakis teaches a microglial dysfunction-associated neurodegenerative disease including AD which has cognitive dysf u nction and short term memory and spatial learning dysfunction as in claims 1-2, 9,12 and 16-17 ( see col. 62, lines 45-50; col.92-93, Example 1 ), the subject has TREM2 deficient cells in the brain prior to administration of the composition as in claims 3, 10 and 18 (see col. 92-col.93, Example 15 ; col. 93, lines 17-39 ); and human as a subject in claims 8, 15 and 20 ( see col. 92-93, Example 15 ) . Fotakis also teaches that wherein the administration of the agonistic anti-Dectin-1 antibody results in improved microglial metabolic activity, decreased microglial autophagy, reduced neurite dystrophy, decreased cell death, improved microglial viability, improved microglia numbers , improved microglia clustering around amyloid beta plaques or reduced plaque-associated neurite dystrophy recited in claims 5-6, 11, 13 because the method of Fotakis uses the same material (i.e. agonistic anti-Dectin-1/CLEC7A antibody) and the same active step (i.e. administering to a subject with AD) in the same patient population (i.e.AD). Thus, claims 1-20 are anti cipated by Fotakis et al. (US12037399). Claim Rejections - 35 USC § 102 12. Claims 1-2 and 5-8 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by Eisenbach-Schwartz et al (US2015/0238582 , as in IDS ) . Eisenbach-Schwartz et al (US2015/0238582 ) teaches a method of treating a disease, disorder, condition or injury of the Central Nervous System (CNS) in a subject in need thereof, comprising administering to the subject a therapeutically effective amount of an active ingredient comprising a Th1 adjuvant ( see [0006]-[0010]; claim 1), wherein the disease is Alzheimer’s disease ( see para. [0002]; claim 35); and the Th1 adjuvant includes an agonist of dectin-1 (see para [0077] ) . Thus, Eisenbach-Schwartz teaches a method of treating Alzheimer’s disease comprising administering a dectin-1 (also called CLEC7A) agonist , which meet the limitations recited in instant claims 1-2 and 5-8 . Eisenbach-Schwartz also teaches t he limitations “wherein the administration of the agonistic anti-Dectin-1 antibody results in improved microglial metabolic activity, decreased microglial autophagy, reduced neurite dystrophy, decreased cell death, improved microglial viability, improved microglia numbers, improved microglia clustering around amyloid beta plaques or reduced plaque-associated neurite dystrophy” recited in claims 5-6 because the method of Eisenbach-Schwartz uses the same material (i.e. dectin-1/CLEC7A agonist) and the same active step (i.e. administering) in the same patient population (i.e. AD) . If the administration of the claimed material can result in the effects recited in claims 5-6 in AD patients, the same material used in the same AD patients in the method of Eisenbach-Schwartz can also achieve the same effects as instantly claimed because the material, the active step and the patient population in the method of Eisenbach-Schwartz are identical to those recited in instant claims. In addition, the se limitations in claims 5-6 are recited in a wherein clause and are inherent results of administering dectin-1 agonist . Therefore, claims 1-2 and 5-8 are anticipated by Eisenbach-Schwartz . C laim Rejections - 35 USC § 103 13. The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action: A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102 of this title, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made. The factual inquiries set forth in Graham v. John Deere Co. , 383 U.S. 1, 148 USPQ 459 (1966), that are applied for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows: 1. Determining the scope and contents of the prior art. 2. Ascertaining the differences between the prior art and the claims at issue. 3. Resolving the level of ordinary skill in the pertinent art. 4. Considering objective evidence present in the application indicating obviousness or nonobviousness. This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention. Claims 1-2 and 5-8 are rejected under 35 U.S.C. 103 as being unpatentable over Eisenbach-Schwartz et al. (US2015/0238582, as in IDS) in view of Oh et al. (US9045542, issued Jun 2, 2015, as in IDS). Eisenbach-Schwartz is set forth above but fai