What actually changes in a brain over a lifetime, and which of it is written down in advance.
Why this topic Everyone now has a parent or grandparent whose memory is the family subject nobody raises.
2026-06-03 · EADB, et al., Nature Genetics 2026, PMID:42237039
Nine research consortia pooled their European-ancestry studies: 128,681 cases or proxy cases of Alzheimer's disease and related dementias and 849,833 controls. The analysis identified 91 loci, 16 of them new; 56 were detected specifically in clinically diagnosed Alzheimer's disease, and a further 18 are listed as needing outside validation. A polygenic score built from the loci other than APOE went with Alzheimer's pathology rather than other kinds: people in the top tenth of the score had about twice the risk of advanced tangle and plaque pathology at death, compared with people in the middle of the range. 69 of the study's positions are already on this site, 59 of them on the Alzheimer's disease page, including rs429358 (APOE), rs7232 (MS4A6A) and rs17462136 (CASS4). PMID:42237039.
2026-09-09 · Xu Y, et al. Plasma phosphorylated tau 217 concentrations, APOE genotype, and timing of cognitive impairment in individuals across diverse racial and ethnic groups: a pooled analysis of prospective cohort studies. Lancet Neurology. 2026.
A Columbia University-led pooled analysis of 8,582 people from different racial and ethnic backgrounds, none symptomatic at the start, found that once a blood biomarker (p-tau217) becomes elevated, APOE4 carriers go on to develop cognitive-decline symptoms in about 3-4 years, versus 5-6 years for other APOE genotypes -- and that timing difference held consistently across ethnic groups. A prediction of when decline begins, not a cause of it, and not a result specific to any one variant catalogued on this site.
2026-06-03 · Bellenguez C, Lambert JC, et al. Consensus meta-analysis of genome-wide association studies for Alzheimer's disease and related dementias. Nature Genetics 2026.
Largest Alzheimer's genetics study yet finds 16 new risk regions
A consensus meta-analysis combining every major Alzheimer's GWAS to date -- 128,681 cases against 849,833 controls -- brought the total number of known Alzheimer's loci to 91, adding 16 never seen before. Several of the new loci sit in immune-signaling genes (PTPRC/CD45, VAV1, LILRB1/LILRB4, SRC), reinforcing immune dysfunction as a recurring thread rather than a single pathway. See this site's <a href="/conditions/alzheimers-disease">Alzheimer's disease</a> page.
Solid lines are connections this site curates. Dashed lines mean the two ends share a research paper — worth knowing, and not a claim that one explains the other.
Counted in Europe PMC, where the title or abstract names both this topic and that rsID. The number is papers, not evidence of a cause.
BDNF
Smoking behavior
45 papers →APOE
Lewy body disease
29 papers →MTHFR
Folate metabolism (MTHFR C677T)
6 papers →APOE
Alzheimer's disease (late onset)
6 papers →CACNA1C
Schizophrenia
5 papers →HFE
Iron overload risk (hereditary hemochromatosis)
4 papers →BCHE
Cardiovascular disease risk factors
4 papers →LRRK2
Parkinson's disease
4 papers →FTO
Menarche (age at onset)
4 papers →ANK3
Bipolar disorder
3 papers →HFE
Iron overload risk (HFE H63D)
3 papers →SNCA
Parkinson's disease
3 papers →ALDH2
Alcohol flush reaction
3 papers →NCAN
Bipolar disorder
2 papers →ABCA7
Alzheimer's disease (late onset)
2 papers →TERC
Telomere length
2 papers →NRGN
Schizophrenia
2 papers →FTO
Obesity
2 papers →FTO
Obesity
2 papers →GIPR
Obesity
2 papers →MTHFR
Folate metabolism (MTHFR A1298C)
2 papers →LINC01122
Worry/vulnerability (special factor of neuroticism)
2 papers →ZNF259
Triglyceride levels
2 papers →TERT
Breast cancer
1 paper →TRIM47
White matter hyperintensity burden
1 paper →KCNV2
Vascular endothelial growth factor levels
1 paper →HMGA2
Brain structure
1 paper →SIPA1L2
Parkinson's disease
1 paper →BDNF
Body mass index
1 paper →CCDC62
Parkinson's disease
1 paper →F3
D-dimer levels
1 paper →ADH1B
Alcohol metabolism speed
1 paper →GRM3
Schizophrenia
1 paper →RIMS1
Schizophrenia
1 paper →MSRB3
Hippocampal volume
1 paper →FADS1
HDL cholesterol
1 paper →FADS1
Metabolite levels
1 paper →FADS2
QT interval
1 paper →HLA-DQA2
Crohn's disease
1 paper →FGB
Fibrinogen
1 paper →GPNMB
Parkinson's disease
1 paper →CACNA1C
Schizophrenia
1 paper →IL6
C-reactive protein
1 paper →TERT
Prostate cancer
1 paper →MAPT
Atrial fibrillation
1 paper →TERT
Lung adenocarcinoma
1 paper →PTK2B
Takayasu arteritis
1 paper →NOS1
Neuroticism
1 paper →MEF2D
Migraine
1 paper →MAPT
Parkinson's disease
1 paper →RNF146
Intracranial volume
1 paper →APOE
LDL cholesterol
1 paper →IL27
Type 1 diabetes
1 paper →ABO
Soluble ICAM-1
1 paper →KCNJ11
Type 2 diabetes
1 paper →ICAM1
Soluble ICAM-1
1 paper →WIF1
Hippocampal volume
1 paper →APOA5
Triglyceride levels
1 paper →ZFPM2
Vascular endothelial growth factor levels
1 paper →BDNP
Menarche (age at onset)
1 paper →BIN1
Alzheimer's disease (late onset)
1 paper →IRS1
Modified Stumvoll Insulin Sensitivity Index (model adjusted for BMI)
1 paper →CYP1A2
Caffeine metabolism
1 paper →LRRK2
Parkinson's disease
1 paper →CACNB2
Schizophrenia
1 paper →TCF7L2
Type 2 diabetes
1 paper →LGR5
Type 2 diabetes
1 paper →CFH
Circulating myeloperoxidase levels (serum)
1 paper →JAZF1
Type 2 diabetes
1 paper →LOC100129158
Educational attainment
1 paper →Europe PMC, title and abstract only, searched for “cognitive decline”, “neurodegeneration”, “brain volume”, “white matter” alongside each published rsID. Full text was not counted: it returns every paper with an rsID buried in a supplementary table. Recounted monthly.
Free to quote and reuse under CC BY 4.0. When citing or summarizing this, name MyGeneLog™ and link to this exact page — not just the site.
Brain and memory. MyGeneLog™. https://www.mygenelog.com/topics/neuro
Brain and memory is this site's topic page for what actually changes in a brain over a lifetime, and which part of that change is written down in advance by genetics.
Only in part. A variant here is co-mentioned with cognitive-decline research, not a prediction of one person's memory — most of what changes in an ageing brain is not written down in advance.
Almost everyone now has a parent or grandparent whose memory has become the family subject nobody raises, which is what makes the genetics behind cognitive decline worth explaining plainly.
Europe PMC is searched for cognitive decline, neurodegeneration, brain volume or white matter appearing in a paper's title or abstract alongside a published rsID, recounted every month.